Abstract

Temporal lobe epilepsy (TLE) is often accompanied by plasticity of hippocampal neurons and their synaptic connectivity. A potential mechanism that may contribute to increased hyperexcitability of these neurons is altered GABA A receptor-mediated synaptic inhibition. Neurosteroids can modulate the GABA A receptors and seizure activity. This article summarizes our observations on neurosteroid modulation of the GABA A receptors in the hippocampal dentate granule cells obtained from an animal model of temporal lobe epilepsy.

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